SP600125 Inhibits Cap-dependent Translation Independently of the c-Jun N-terminal Kinase Pathway

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  • Ito Masatoshi
    Laboratory for Immunogenomics, RIKEN Research Center for Allergy and Immunology Department of Supramolecular Biology, Graduate School of Nanobioscience, Yokohama City University
  • Kitamura Hiroshi
    Laboratory for Immunogenomics, RIKEN Research Center for Allergy and Immunology Department of Comparative and Experimental Medicine, Graduate School of Medical Sciences, Nagoya City University
  • Kikuguchi Chisato
    Laboratory for Immunogenomics, RIKEN Research Center for Allergy and Immunology
  • Hase Koji
    Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology
  • Ohno Hiroshi
    Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology Department of Supramolecular Biology, Graduate School of Nanobioscience, Yokohama City University
  • Ohara Osamu
    Laboratory for Immunogenomics, RIKEN Research Center for Allergy and Immunology Department of Human Genome Research, Kazusa DNA Research Institute

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説明

We investigated the effects of SP600125 (formerly called c-Jun N-terminal kinase (JNK) inhibitor II) on translation using cultured mouse cells. SP600125 (50 μM) treatment rapidly repressed overall protein synthesis, accompanied by a reduction in the mRNAs for housekeeping genes such as glyceraldehyde-3-phosphate dehydrogenase in the polysomal fraction. SP600125 decreased polysomes with a concomitant increase in free ribosomal subunits in the cytoplasm, suggesting that global translation was inhibited at the initiation step. A reporter analysis using exogenous mRNAs showed that SP600125 inhibited cap-dependent but not internal ribosome entry site-dependent translation. SP600125 significantly attenuated phosphorylation of components in the mTOR pathway, which is responsible for cap-dependent translation. In contrast to SP600125, short hairpin RNAs for JNK1 and JNK2 failed to affect overall protein synthesis. Collectively, SP600125 inhibits cap-dependent translation, independent of the JNK pathway.<br>

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